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Targeting neurodegenerative disease-associated protein aggregation with proximity-inducing modalities

Acta Pharmacologica Sinica volume 46, pages 2337–2346 (2025)Cite this article

Abstract

Neurodegenerative diseases (NDDs) are characterized by progressive neuronal dysfunction and anatomical changes caused by neuron loss and gliosis, ultimately leading to severe declines in brain function. While these disorders arise from a variety of pathological mechanisms, a common molecular feature is the accumulation of misfolded proteins, which occurs both inside and outside neurons. For example, Alzheimer’s disease (AD) is defined by extracellular β-amyloid plaques and intracellular tau neurofibrillary tangles. These pathological protein aggregates are often resistant to traditional small molecule drugs. Recent advances in proximity-inducing chimeras such as proteolysis-targeting chimeras (PROTACs), lysosome-targeting chimeras (LYTACs), autophagy-targeted chimeras (AUTOTACs), dephosphorylation-targeting chimeras (DEPTACs) and ribonuclease-targeting chimeras (RIBOTACs) offer promising strategies to eliminate pathological proteins or mRNAs through intracellular degradation pathways. These innovative approaches open avenues for developing new therapies for NDDs. In this review we summarize the regulatory mechanisms of protein aggregation, highlight the advancements in proximity-inducing modalities for NDDs, and discuss the current challenges and future directions in therapeutic development.

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Fig. 1: Schematic illustration of the mechanisms and applications of proximity-inducing modalities against NDDs.
Fig. 2: Schematic illustration of the PROTAC-mediated protein degradation mechanisms.
Fig. 3: Schematic illustration of HyT-mediated protein degradation mechanisms and the representative chemicals.
Fig. 4: Schematic diagrams indicating the structure and mechanisms of action of the TRIM21-based modalities.
Fig. 5: Schematic illustration of the mechanisms of action of AUTOTAC, ATTEC, and CMATAC.
Fig. 6: Schematic illustration of the mechanisms of action of DEPTAC and the chemicals of tau DEPTACs.
Fig. 7: Schematic illustration of the mechanisms of action of RIBOTAC and the representative chemicals.

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Acknowledgements

This work was supported by grants from the National Natural Science Foundation of China (32270892 and 32200613) and the Shandong Provincial Natural Science Foundation (ZR2021MC157).

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Authors and Affiliations

  1. Center for Cell Structure and Function, Collaborative Innovation Center of Cell Biology in Universities of Shandong, College of Life Sciences, Shandong Normal University, Jinan, 250014, China

    Rui-xin Ge, Qing-chao Li, Min Liu & Jun Zhou

  2. School of Life Sciences and Medicine, Shandong University of Technology, Zibo, 255500, China

    Miao Chen

  3. State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Science, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, 300071, China

    Jun Zhou

  4. The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Medical University. Department of Ophthalmology, Ministry of Education International Joint Laboratory of Ocular Diseases, Tianjin Key Laboratory of Ocular Trauma, Tianjin Institute of Eye Health and Eye Diseases, China-UK “Belt and Road” Ophthalmology Joint Laboratory, Tianjin Medical University General Hospital, Tianjin, 300052, China

    Song-bo Xie

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Ge, Rx., Chen, M., Li, Qc. et al. Targeting neurodegenerative disease-associated protein aggregation with proximity-inducing modalities. Acta Pharmacol Sin 46, 2337–2346 (2025). https://doi.org/10.1038/s41401-025-01538-2

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